Promoter polymorphisms in the lncRNA-MIAT gene associated with acute myocardial infarction in Chinese Han population:

Ruchao Ma1,2, Xiaohui He1, Xiaoyun Zhu3

  • 1Shandong University Cheeloo College of Medicine, Jinan, Shandong 250012, China.

Bioscience Reports
|February 25, 2020
PubMed

Insights

Genetic variations in the MIAT gene promoter, specifically rs5752375 and rs9608515, are linked to acute myocardial infarction (AMI) in the Chinese Han population. These findings may aid in the early diagnosis of AMI.

Area of Science:

  • Genetics
  • Cardiovascular Disease Research
  • Molecular Biology

Background:

  • Coronary atherosclerotic disease (CAD) is a leading global cause of mortality and morbidity.
  • Acute myocardial infarction (AMI) represents the most severe manifestation of CAD.
  • The myocardial infarction (MI) associated transcript (MIAT) long non-coding RNA plays a crucial role in AMI pathogenesis.

Purpose of the Study:

  • To investigate the association between polymorphisms in the MIAT gene promoter and AMI.
  • To analyze these associations within the Chinese Han population.

Main Methods:

  • Recruited 212 AMI patients and 218 healthy controls.
  • Utilized polymerase chain reaction (PCR) and sequencing to identify MIAT promoter single nucleotide polymorphisms (SNPs).
  • Employed chi-square tests, logistic regression, and SHEsis software for statistical analysis, linkage disequilibrium, and haplotype analysis.

Main Results:

  • Identified ten SNPs in the MIAT promoter region.
  • Found significant associations between AMI and two specific SNPs: rs5752375 and rs9608515.
  • Observed that these associated polymorphisms might alter transcription factor binding sites within the MIAT promoter.

Conclusions:

  • MIAT promoter polymorphisms rs5752375 and rs9608515 are significantly associated with AMI in the Chinese Han population.
  • These genetic markers hold potential clinical importance for the early diagnosis of AMI.
  • Further research into MIAT's role in AMI pathogenesis is warranted.
Abstract

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